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GWAS Study

Genetic and clinical determinants of abdominal aortic diameter: genome-wide association studies, exome array data and Mendelian randomization study.

Portilla-Fernandez E, Klarin D, Hwang SJ et al.

35234888 PubMed ID
GWAS Study Type
13542 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

PE
Portilla-Fernandez E
KD
Klarin D
HS
Hwang SJ
BM
Biggs ML
BJ
Bis JC
WS
Weiss S
RS
Rospleszcz S
NP
Natarajan P
HU
Hoffmann U
RI
Rogers IS
TQ
Truong QA
VU
Völker U
DM
Dörr M
BR
Bülow R
CM
Criqui MH
AM
Allison M
GS
Ganesh SK
YJ
Yao J
WM
Waldenberger M
BF
Bamberg F
RK
Rice KM
EJ
Essers J
KD
Kapteijn DMC
VD
van der Laan SW
DK
de Knegt RJ
GM
Ghanbari M
FJ
Felix JF
IM
Ikram MA
KM
Kavousi M
UA
Uitterlinden AG
RA
Roks AJM
DA
Danser AHJ
TP
Tsao PS
DS
Damrauer SM
GX
Guo X
RJ
Rotter JI
PB
Psaty BM
KS
Kathiresan S
VH
Völzke H
PA
Peters A
JC
Johnson C
SK
Strauch K
MT
Meitinger T
OC
O'Donnell CJ
DA
Dehghan A
Chapter II

Abstract

Summary of the research findings

Progressive dilation of the infrarenal aortic diameter is a consequence of the ageing process and is considered the main determinant of abdominal aortic aneurysm (AAA). We aimed to investigate the genetic and clinical determinants of abdominal aortic diameter (AAD). We conducted a meta-analysis of genome-wide association studies in 10 cohorts (n = 13 542) imputed to the 1000 Genome Project reference panel including 12 815 subjects in the discovery phase and 727 subjects [Partners Biobank cohort 1 (PBIO)] as replication. Maximum anterior-posterior diameter of the infrarenal aorta was used as AAD. We also included exome array data (n = 14 480) from seven epidemiologic studies. Single-variant and gene-based associations were done using SeqMeta package. A Mendelian randomization analysis was applied to investigate the causal effect of a number of clinical risk factors on AAD. In genome-wide association study (GWAS) on AAD, rs74448815 in the intronic region of LDLRAD4 reached genome-wide significance (beta = -0.02, SE = 0.004, P-value = 2.10 × 10-8). The association replicated in the PBIO1 cohort (P-value = 8.19 × 10-4). In exome-array single-variant analysis (P-value threshold = 9 × 10-7), the lowest P-value was found for rs239259 located in SLC22A20 (beta = 0.007, P-value = 1.2 × 10-5). In the gene-based analysis (P-value threshold = 1.85 × 10-6), PCSK5 showed an association with AAD (P-value = 8.03 × 10-7). Furthermore, in Mendelian randomization analyses, we found evidence for genetic association of pulse pressure (beta = -0.003, P-value = 0.02), triglycerides (beta = -0.16, P-value = 0.008) and height (beta = 0.03, P-value < 0.0001), known risk factors for AAA, consistent with a causal association with AAD. Our findings point to new biology as well as highlighting gene regions in mechanisms that have previously been implicated in the genetics of other vascular diseases.

12,815 European ancestry individuals

Chapter III

Study Statistics

Key metrics and study information

13542
Total Participants
GWAS
Study Type
Yes
Replicated
727 European ancestry individuals
Replication Participants
European
Ancestry
Netherlands, U.S., Germany
Recruitment Country
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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